This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The goal of this project is to establish the role of p53 protein in early kidney development, as aberrations during the early stages of development can lead to congenital defects. Recent studies show that loss of p53 in mice embryos causes kidney structure and growth abnormalities (kidney/ureter duplication, obstruction of ureter). Infants born with duplex kidneys may suffer from unilateral or bilateral vesicoureteral reflux, hydronephrosis, and cystic-dysplasia.